Excitingly, CS1 and CS2 were also highly effective in inhibiting AML differentiation and the FTO signaling pathways, as well as in sensitizing AML cells to T cell cytotoxicity by decreasing the expression of leukocyte immunoglobulin-like receptor subfamily B 4 (LILRB4), thus overcoming immune evasion [419]. This evidence concerns the gene LILRB4 and acute myeloid leukemia.